Evidence map›Paper›PMID 18562483›Full record

ArticleAmerican journal of physiology. Cell physiology2008

oxLDL facilitates flow-induced realignment of aortic endothelial cells.

Gregory B Kowalsky, Fitzroy J Byfield, Irena Levitan

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.8field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
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  9. oxLDL induces endothelial cell proliferation via Rho/ROCK/Akt/p27American journal of physiology. Cell physiology · 2017
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  18. Cholesterol depletion facilitates recovery from hypotonic cell swelling in CHO cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2011
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Gregory B KowalskySection of Pulmonary, Critical Care, and Sleep Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA.
Fitzroy J Byfield
Irena Levitan
California University of Pennsylvania · USUniversity of Illinois Chicago · US

Funding

Cholesterol Regulation of Endothelial K+ ChannelsR01HL073965 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI LEVITAN, IRENA · 2004 to 2024
$7.3M
Impact of dyslipidemia on endothelial biomechanicsR01HL083298 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LEVITAN, IRENA, MINSHALL, RICHARD D · 2007 to 2021
$7.0M
NHLBI NIH HHS HL-073965NHLBI NIH HHS HL-083298NHLBI NIH HHS R01 HL073965NHLBI NIH HHS R01 HL083298
6 · The paper itself

Abstract

Alignment of vascular endothelial cells (ECs) in the direction of the flow is considered a key factor in maintaining endothelial integrity in an active hemodynamic environment. Our recent studies showed that exposure to oxidized LDL (oxLDL), one of the major proatherogenic lipoproteins, significantly increases the stiffness of human aortic ECs, suggesting that oxLDL may have a significant impact on the sensitivity of ECs to mechanical stimuli. In this study, we show that oxLDL strongly enhances the ability of ECs to realign in the direction of the flow and facilitates the formation of F-actin stress fibers under static and flow conditions. The impact of oxLDL on the flow-induced realignment is observed on whole cell and single-fiber levels. We also show that, similar to the effect of oxLDL on endothelial stiffness, the impact of oxLDL on flow-induced realignment can be simulated by methyl-beta-cyclodextrin-induced cholesterol depletion, supporting the hypothesis that oxLDL acts as cholesterol acceptor, rather than cholesterol donor, for ECs. Finally, we propose that oxLDL/cholesterol depletion-induced sensitization of ECs to flow may be a result of an increase in cellular stiffness and a respective increase in membrane-cytoskeleton tension.

Indexed as

AnimalsAortabeta-CyclodextrinsCattleCells, CulturedCell ShapeCholesterolElasticityEndothelial CellsHumansLipoproteins, LDLRheologyStress Fibersacetyl-LDLbeta-CyclodextrinsCholesterolLipoproteins, LDLmethyl-beta-cyclodextrinoxidized low density lipoprotein

Identifiers

PMID18562483
PMCPMC2518412
OpenAlexW2062972876

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.